The present invention relates to a pharmaceutical product comprising a parasympathomimetic drug having therapeutic properties on the pathology of human sensitivity and of the motor system in general.
Parasympathomimetic drugs are already known, the effect of which is similar to that which is obtained by stimulating the parasympathetic postganglionic fibres.
The fact is also known that these drugs are at present rarely used since their action throughout the sensory periphery is little known.
In this connection it should be pointed out that the applicant has elaborated a theory about a "sympathetic-sensory coupling" (SSC), by postulating ubiquitous sympathetic inhibitions throughout the sensory periphery.
Considering the well-known sympathetic-parasympathetic parallelism on smooth muscle, glands and myocardium, the same applicant has experimentally exploited the parasympathetic denervation supersensitivity of familial dysautonomia (Riley-Day disease) and he has reversed with parasympathomimetic drugs the skin and corneal analgesia, the ageusia, anosmia and proprioceptive and vestibular areflexia of this disease, thus experimentally showing for the first time the existence of excitatory "parasympathetic-sensory couplings" (PSC).
Moreover, he has integrated this discovery the general theory of the "sympathetic and parasympathetic sensory coupling" (SPSC), and into the essential distinction between the following peripheries:
1) normechanoceptive, nornociceptive, norproprioceptive and
2) dysmechanoceptive, dysnociceptive, dysproprioceptive.
This theory postulates the existence of normal normechanoceptors, nornociceptors and norproprioceptors which are excited by the parasympathetic system and inhibited by the sympathetic one; and that, "in the case of a parasympathetic denervation, parasympathetic drugs can replace the excitatory action of the parasympathetic system thereon.
Vice versa, in the case of a biochemical alteration of the axoplasmic flow of the primary sensory neurons, due to a central or peripheral cause, these neurons may display membrane dysmetabolic characteristics which transform normechanoceptors into dysmechanoceptors, nornociceptors into dysnociceptors, and norproprioceptors into dysproprioceptors.
On these dysmechanoceptors, dysnociceptors and dysproprioceptors, the parasympathetic nervous system reverses its action, from being excitatory on to the normechanoceptors, nornociceptors and norproprioceptors, into being an inhibitory one.
However, the parasympathetic action becomes very small or absent, because of the prevalence of an excitatory action of the sympathetic nervous system on dysmechanoceptors, dysnociceptors and dysproprioceptors.